Benzodiazepine dependence — structured taper after withdrawal seizure (MEQ)

(i) Mechanism and unsafe abrupt stop. Alprazolam is a high-potency, relatively short-acting GABA-A positive allosteric modulator. Chronic exposure produces tolerance via receptor adaptation; abrupt loss of cover unmasks CNS hyperexcitability — anxiety, autonomic arousal, and lowered seizure threshold. A GTCS after 48 hours off short-acting BZD is classic severe withdrawal, not proof he can “white-knuckle” to zero. Physiological dependence is expected after years of multi-milligram daily use, including illicit top-ups.[1][3]

(ii) Immediate management. ABC already stabilised; exclude other seizure causes (done: CT, electrolytes, low alcohol now — still take full alcohol history and withdrawal risk). Reinstate benzodiazepine cover at a dose sufficient to suppress severe withdrawal, then transition to a controlled taper — do not honour a same-day total stop after a seizure. Assess alcohol use disorder severity, CIWA-type needs if still withdrawing from alcohol, thiamine if alcohol dependence, and dual-diagnosis supports. Screen for other substances, suicide risk, driving ban after seizure per local rules, and capacity for shared decisions once clear.[2][1]

(iii) Taper plan. Prefer conversion of alprazolam to approximate diazepam equivalents for smoother reductions and tablet flexibility; stabilise 24–72 hours (or longer if high dose/complex), then reduce gradually — commonly about 5–10% every 1–2 weeks, slower at low doses, hold if severe symptoms. High daily dose, illicit supply, alcohol co-use, and seizure history favour inpatient or closely supervised start. Monitor withdrawal symptoms, mood, alcohol substitution, sleep, and seizure recurrence. Document a written plan with the GP and prescription-monitoring review.[2][6][3]

(iv) Z-drugs and supports. Zolpidem is not a non-addictive long-term fix; Z-drugs act at related GABA-A BZ sites and can cause dependence and complex sleep behaviours. Offer CBT-I / sleep hygiene and treat panic/anxiety with evidence-based non-BZD approaches. Psychosocial interventions help harmful BZD use; patient education deprescribing models (EMPOWER) and BRZA deprescribing guidance support structured conversations; joint tapering CPG frames when risks outweigh benefits.[4][5][7][6]

(v) Opioid counselling. Even without current opioids, counsel that future opioid–BZD combinations synergistically depress respiration and raise overdose death risk — critical harm-reduction content given his polydrug trajectory.[8][1]